The Frederick Anokye-Danso Lab investigates the biological pathways at work in the separation of human pluripotent stem cells into adipocytes and pancreatic beta cells. We focus in particular on determinant factors of obesity and metabolic dysfunction, such as the P72R polymorphism of p53. We also conduct research on the reprogramming of somatic cells into pluripotent stem cells using miRNAs.

The Todd Brown Lab focuses on metabolic, endocrine and skeletal abnormalities in HIV-infected patients, particularly as these factors relate to aging. Our studies take an epidemiologic approach to understanding the occurrence and prevalence of insulin resistance, diabetes, and anthropometric changes in HIV patients and their relationship to antiretroviral treatment.

Research in the Rita Kalyani Lab examines the decreased physical functioning observed in patients with diabetes as they age. Through several ongoing epidemiological cohorts, we are investigating the association of high blood glucose and high insulin levels with accelerated muscle loss, and possible contributions to the physical disability observed in diabetes. We are currently involved in clinical studies that aim to understand the underlying mechanisms for these associations and to facilitate the development of novel strategies to prevent muscle loss and disability in people with diabetes.

Our research aims to expand the understanding of how hormones regulate pancreatic islets in health and disease. Currently, a major focus of the lab is to define the normal adaptations of islets, particularly insulin-producing beta-cells, to the metabolic stress of pregnancy, and to determine how defective adaptation contributes to gestational diabetes mellitus (GDM). We anticipate that elucidating physiologic mechanisms of gestational beta-cell adaptation will identify novel therapeutic strategies to expand functional beta-cell mass which would help in the treatment of all types of diabetes.

The Melia lab performs basic, translational, and clinical research on inflammatory bowel disease. Specifically, Dr Melia's basic science and translational research program is concentrated on novel roles of manganese (Mn) homeostasis in Crohn's disease and the interaction with aberrant N-glycosylation with current support from NIDDK and NICHD, including support as a co-investigator in the Center for Metals in Nutrition and Development.

Research in the Noah Lechtzin Lab investigates several important aspects of cystic fibrosis (CF), including the impact of antibiotic-resistant bacterial infections in CF patients and new therapy options for individuals with CF. Our research into new CF therapies has included studies on home electronic symptom and lung function monitoring, transbronchial needle aspiration and bedside percutaneous endoscopic gastrostomy tube placement. We also explore the role of metabolic complications in CF patients by examining how the disease is impacted by factors such as vitamin D deficiency, osteoporosis and testosterone deficiency.

Founded in the late 1980s, our Lab explores the fundamental mechanisms of neural responses to traumatic and degenerative signals and works to identify targets for treating injury/degeneration with small molecules, peptides and cells. We currently focus on traumatic and degenerative axonopathies as they occur in traumatic brain injury (diffuse axonal injury), neurodegenerative diseases i.e. Alzheimer's disease and other white matter conditions, e.g. hypoxic ischemic encephalopathy, demyelination. We are especially interested in the role of the MAPK cascade of injury, NAD metabolism and SARM1 signaling and their convergence on Wallerian degeneration.

The Foster Lab uses the tools of protein biochemistry and proteomics to tackle fundamental problems in the fields of cardiac preconditioning and heart failure. Protein networks are perturbed in heart disease in a manner that correlates only weakly with changes in mRNA transcripts. Moreover, proteomic techniques afford the systematic assessment of post-translational modifications that regulate the activity of proteins responsible for every aspect of heart function from electrical excitation to contraction and metabolism. Understanding the status of protein networks in the diseased state is, therefore, key to discovering new therapies. D. Brian Foster, Ph.D., is an assistant professor of medicine in the division of cardiology, and serves as Director of the Laboratory of Cardiovascular Biochemistry at the Johns Hopkins University School of Medicine.

Our laboratory conducts basic and translational research aimed at better understanding the pathogenesis of multiple sclerosis (MS) and the role of the immune system in CNS disease, particularly the processes that drive progressive disability such as neurodegeneration and remyelination failure. We currently have three parallel research programs: 1. Metabolism as a modulator of MS: We are studying how basic metabolic pathways regulate the immune system and how these pathways might be exploited to protect neurons and myelin-forming oligodendrocytes from injury. 2. Identifying pathways by which nitric oxide (NO) and other free radicals cause neuronal and axonal damage. Our lab is identifying specific signaling pathways initiated by NO and other free radicals that can be targeted by drugs to produce neuroprotection. 3. Modulating the innate immune system in MS: In collaboration with others at Johns Hopkins, we are studying ways to enhance the reparative functions of microglia while preventing maladaptive responses. This work has identified bryostatin-1 as a potential drug that may be re-purposed for this task.

The Theresa Shapiro Laboratory studies antiparasitic chemotherapy. On a molecular basis, we are interested in understanding the mechanism of action for existing antiparasitic agents, and in identifying vulnerable metabolic targets for much-needed, new, antiparasitic chemotherapy. Clinically, our studies are directed toward an evaluation, in humans, of the efficacy, pharmacokinetics, metabolism and safety of experimental antiparasitic drugs.